Ikaros and HDACs interaction in CLL human derived cell lines (MEC-1 and MEC-2)

• Grant number: 19/05147-6
• Support Opportunities: Scholarships in Brazil - Scientific Initiation
• Start date: June 01, 2019
• End date: December 31, 2019
• Field of knowledge: Biological Sciences - Immunology
• Principal Investigator: Ana Flavia Popi
• Grantee: Julia Caroline Mourão de Souza
• Host Institution: Escola Paulista de Medicina (EPM). Universidade Federal de São Paulo (UNIFESP). Campus São Paulo. São Paulo , SP, Brazil

Abstract

Chronic lymphatic leukemia (CLL) is a hematopoietic hyperproliferative disease caused by deregulated B-1 cells (CD5+) expansion. Our group demonstrated that CLL cells show dysfunction and altered localization of Ikaros. This protein acts by repressing or activating the gene expression. Ikaros is associated to a protein complex that is able to remodel the chromatin. The major complex that interacts to Ikaros is NuRD, where the histones deacetylases enzymes (HDACs) are an important component. HDACs are a vast family of enzymes responsible by repressing the transcription of genes due to the ability to compact the nucleosome. This study aims to evaluate if the alterations in Ikaros detected in CLL cells could be related to modifications in the expression and their interaction with HDACs. This interaction will be studied in human CLL-derived cell lines: MEC-1 and MEC-2.